Scars, burns & healing最新文献

Introduction: Keloid scars are a particularly challenging clinical entity and a variety of management approaches have been described in the literature including intralesional surgery. The current literature lacks a summative review to ascertain the evidence base behind this surgical approach.

Methods: A comprehensive English literature database search was performed using PubMed Medline, EMBASE and Web of Science from their individual dates of inception to March 2018. We present the different rationales proposed for the use of this technique, the clinical outcomes reported in the literature as well as the scientific basis for intralesional excision of keloid scars.

Discussion: A number of arguments have been proposed to support intralesional excision including avoiding injury to neighbouring non-keloidal skin and the deep layer of the dermis, removal of the most proliferative fibroblastic group as well as debulking to facilitate the administration of injectable steroid. The most current literature does not provide sufficient support for the adoption of intralesional excisions based on data emerging from basic science as well as clinical outcome studies.

Conclusion: Emerging evidence supports the extralesional excision of keloid scars based on current mechanobiological, histological as well as clinical outcome data. Further trials comparing extralesional and intralesional surgical practices are eagerly awaited to ascertain the role of intralesional excisions in the keloid management arena.

Background: In contrast to fetal scar tissue, adult scar tissue presents with visible scarring. Topical silicone creams have been shown to improve the appearance of scars. This case series compares the genetic expression of post-surgical scar tissues that received topical scar treatment with silicone cream, SKN2017B, or no treatment. SKN2017B is a recently formulated silicone-based scar cream that contains selective synthetic recombinant human growth factors, hyaluronic acid, and vitamin C. We hypothesise that scars treated with silicone-based scar creams have a more favourable genetic expression resembling a well-healing scar.

Methods: Women who had undergone an abdominoplasty were included in this investigation and randomly assigned to treat part of the scar with topical silicone, another part with SKN2017B, and to leave a third part untreated. After four weeks, punch biopsies were taken and the RNA sequenced. Healthy abdominal skin was biopsied as baseline data. Genes of interest were identified and median values were calculated for the samples.

Results: SKN2107B-treated scars demonstrated the lowest collagen type I to collagen type III ratio. Other key genes of interest in wound healing showed the lowest (favourable) expression of fibroblast activation protein alpha, lysyl oxidase and cartilage oligomeric matrix protein; the highest (favourable) expression of fibronectin type III domain containing 1 and matrix metallopeptidase 9 were found in scars treated with SKN2017B.

Conclusion: The results of this small case series demonstrate a trend that those scars treated with topical silicone cream, notably SKN2017B, display the most favourable gene expression for wound healing.

Introduction: Keloids and hypertrophic scars are fibroproliferative disorders of the skin that result from abnormal healing of injured or irritated skin. Multiple studies suggest that genetic, systemic and local factors may contribute to the development and/or growth of keloids and hypertrophic scars. A key local factor may be mechanical stimuli. Here, we provide an up-to-date review of the studies on the roles that genetic variation, epigenetic modifications and mechanotransduction play in keloidogenesis.

Methods: An English literature review was performed by searching the PubMed, Embase and Web of Science databases with the following keywords: genome-wide association study; epigenetics; non-coding RNA; microRNA; long non-coding RNA (lncRNA); DNA methylation; mechanobiology; and keloid. The searches targeted the time period between the date of database inception and July 2018.

Results: Genetic studies identified several single-nucleotide polymorphisms and gene linkages that may contribute to keloid pathogenesis. Epigenetic modifications caused by non-coding RNAs (e.g. microRNAs and lncRNAs) and DNA methylation may also play important roles by inducing the persistent activation of keloidal fibroblasts. Mechanical forces and the ensuing cellular mechanotransduction may also influence the degree of scar formation, scar contracture and the formation/progression of keloids and hypertrophic scars.

Conclusions: Recent research indicates that the formation/growth of keloids and hypertrophic scars associate clearly with genetic, epigenetic, systemic and local risk factors, particularly skin tension around scars. Further research into scar-related genetics, epigenetics and mechanobiology may reveal molecular, cellular or tissue-level targets that could lead to the development of more effective prophylactic and therapeutic strategies for wounds/scars in the future.